A computational approach to flame hole dynamics

Turbulent diffusion flames at low strain rates sustain a spatially continuous flame surface. However, at high strains, which may be localized in a flow or not, the flame can be quenched due to the increased heat loss away from the reaction zone. These quenched regions are sometimes called flame holes. Flame holes reduce the efficiency of combustion, can increase the production of certain pollutants (e.g. carbon monoxide, soot) as well as limit the overall stability of the flame. We present a numerical algorithm for the calculation of the dynamics of flame holes in diffusion flames. The key element is the solution of an evolution equation defined on a general moving surface. The low-dimensional manifold (the surface) can evolve in time and it is defined implicitly as an iso-level set of an associated Cartesian scalar field. An important property of the method described here is that the surface coordinates or parameterization does not need to be determined explicitly; instead, the numerical method employs an embedding technique where the evolution equation is extended to the Cartesian space, where well-known and efficient numerical methods can be used. In our application of this method, the field defined on the surface represents the chemical activity state of a turbulent diffusion flame. We present a formulation that describes the formation, propagation, and growth of flames holes using edge-flame modeling in laminar and turbulent diffusion flames. This problem is solved using a high-order finite-volume WENO method and a new extension algorithm defined in terms of propagation PDEs. The complete algorithm is demonstrated by tracking the dynamics of flame holes in a turbulent reacting shear layer. The method is also implemented in a generalized unstructured low-Mach number fluid solver (Sandia's SIERRA low Mach Module ``Nalu") and applied to simulate local extinction in a piloted jet diffusion flame configuration

Incomplete risk adjustment and adverse selection in the German public health insurance system

"The German statutory health insurance market was exposed to competition in 1996. To avoid adverse selection, a prospective risk compensation scheme was introduced in 1994. Due to their low contribution rates, company-based sickness funds were able to attract a lot of new members. We analyze - using data from the German Socio-Economic Panel - the determinants of these transitions from 1995 to 2000. By estimating a simultaneous two equation system, we find that health status positively, and significantly, affects the probability of changing to a company-based sickness fund, especially after controlling for age. Thus the risk compensation scheme does not fully control for the health status of the changers. Consequently, the comparative advantages of company-based funds will increase over time. This observation provides evidence for the standard Rothschild-Stiglitz separating equilibrium." (author's abstract)"In der Gesetzlichen Krankenversicherung wurde 1996 Wettbewerb zwischen den Krankenkassen eingeführt. Um Adverse Selektion zu verhindern wurde 1994 ein prospektiver Risikostrukturausgleich eingeführt. Aufgrund ihrer niedrigen Beitragssätze konnten die Betriebskrankenkassen eine Vielzahl neuer Mitglieder gewinnen. Wir nutzen Daten des Sozio-oekonomischen Panels (SOEP), um diese Wechselbewegungen für den Zeitraum von 1995 bis 2000 zu analysieren. Ein Zweigleichungssystem wird simultan geschätzt. Es zeigt sich, dass der Gesundheitszustand, nachdem insbesondere für Alter kontrolliert wurde, die Wahrscheinlichkeit zu einer Betriebskrankenkasse zu wechseln signifikant positiv beeinflusst. Der Risikostrukturausgleich gleicht also Unterschiede im Gesundheitszustand nicht vollständig aus. Die komparativen Wettbewerbsvorteile der Betriebskrankenkassen werden somit über die Zeit ansteigen. Dies liefert Evidenz für das bekannte separierende Gleichgewicht von Rothschild und Stiglitz." (Autorenreferat

Control of hypothalamic-pituitary-adrenal stress axis activity by the intermediate conductance calcium-activated potassium channel, SK4

NON-TECHNICAL SUMMARY: Our ability to respond to stress is critically dependent upon the release of the stress hormone adrenocorticotrophic hormone (ACTH) from corticotroph cells of the anterior pituitary gland. ACTH release is controlled by the electrical properties of corticotrophs that are determined by the movement of ions through channel pores in the plasma membrane. We show that a calcium-activated potassium ion channel called SK4 is expressed in corticotrophs and regulates ACTH release. We provide evidence of how SK4 channels control corticotroph function, which is essential for understanding homeostasis and for treating stress-related disorders. ABSTRACT: The anterior pituitary corticotroph is a major control point for the regulation of the hypothalamic–pituitary–adrenal (HPA) axis and the neuroendocrine response to stress. Although corticotrophs are known to be electrically excitable, ion channels controlling the electrical properties of corticotrophs are poorly understood. Here, we exploited a lentiviral transduction system to allow the unequivocal identification of live murine corticotrophs in culture. We demonstrate that corticotrophs display highly heterogeneous spontaneous action-potential firing patterns and their resting membrane potential is modulated by a background sodium conductance. Physiological concentrations of corticotrophin-releasing hormone (CRH) and arginine vasopressin (AVP) cause a depolarization of corticotrophs, leading to a sustained increase in action potential firing. A major component of the outward potassium conductance was mediated via intermediate conductance calcium-activated (SK4) potassium channels. Inhibition of SK4 channels with TRAM-34 resulted in an increase in corticotroph excitability and exaggerated CRH/AVP-stimulated ACTH secretion in vitro. In accordance with a physiological role for SK4 channels in vivo, restraint stress-induced plasma ACTH and corticosterone concentrations were significantly enhanced in gene-targeted mice lacking SK4 channels (Kcnn4(−/−)). In addition, Kcnn4(−/−) mutant mice displayed enhanced hypothalamic c-fos and nur77 mRNA expression following restraint, suggesting increased neuronal activation. Thus, stress hyperresponsiveness observed in Kcnn4(−/−) mice results from enhanced secretagogue-induced ACTH output from anterior pituitary corticotrophs and may also involve increased hypothalamic drive, thereby suggesting an important role for SK4 channels in HPA axis function

Assessment of arterial stiffness, oxidative stress and inflammation in acute kidney injury

Background: It is well know that arterial stiffness, oxidative stress and inflammation are features of chronic kidney disease. The arterial changes have a multitude of potential interconnected causes including endothelial dysfunction, oxidative stress, inflammation, atherosclerosis and vascular calcification. There is evidence that arterial stiffness becomes progressively worse as CKD progresses. The contribution of the biochemical changes of uremic toxicity to arterial stiffness is less clear. The aim of this study is to elucidate the vascular changes in acute kidney injury. We hypothesise that arterial stiffness will be increased during acute kidney injury and this will return to normal after kidney function recovers

Curves of Placental Weights of Live-Born Twins

The purpose of this study is to present curves of estimated placental growth in twins and to evaluate the relative contribution of gestational age, zygosity, chorionicity, fusion of the placentas, sex of the individual and of the twin pair, site of the umbilical cord insertion, birth order, maternal age, and parity. Perinatal data and placental data were obtained from 6315 live-born twin pairs from the East Flanders Prospective Twin Survey. Of 4318 twin pairs, with no missing values, the placental weights of different gestational ages were analyzed using a nonlinear multivariate Gaussian regression. Two groups were distinguished: (1) twins with two separate placentas, and (2) twins with only one placental mass (one placenta in case of monochorionic twins or two fused placentas in case of dichorionic placentas). Overall, placental weight was influenced by gestational age, fusion of the placentas, and parity. In the case of one placental mass, monozygotic dichorionic twins had the lowest weights. If two separate placentas were present, birth order played a role in favor of the first-born twin. For parity and zygosity, the differences were most pronounced between 27 and 29 weeks, whereas the difference for birth order was most pronounced between 33 and 37 weeks. In conclusion, basic physiological characteristics, routinely examined at birth, influence placental weight. Taking these covariates into account allows a better evaluation of the placental weight given a gestational age, as an indicator of growth

Plasma protein C levels in immunocompromised septic patients are significantly lower than immunocompetent septic patients: a prospective cohort study

Introduction: Activated Protein C [APC] improves outcome in immunocompetent patients with severe sepsis particularly in those who are perceived to have high mortality risk. Before embarking on a trial of APC administration in immunocompromised septic patients, a preliminary study on plasma levels of protein C in this cohort is essential

The Brain-Specific Beta4 Subunit Downregulates BK Channel Cell Surface Expression

The large-conductance K+ channel (BK channel) can control neural excitability, and enhanced channel currents facilitate high firing rates in cortical neurons. The brain-specific auxiliary subunit β4 alters channel Ca++- and voltage-sensitivity, and β4 knock-out animals exhibit spontaneous seizures. Here we investigate β4's effect on BK channel trafficking to the plasma membrane. Using a novel genetic tag to track the cellular location of the pore-forming BKα subunit in living cells, we find that β4 expression profoundly reduces surface localization of BK channels via a C-terminal ER retention sequence. In hippocampal CA3 neurons from C57BL/6 mice with endogenously high β4 expression, whole-cell BK channel currents display none of the characteristic properties of BKα+β4 channels observed in heterologous cells. Finally, β4 knock-out animals exhibit a 2.5-fold increase in whole-cell BK channel current, indicating that β4 also regulates current magnitude in vivo. Thus, we propose that a major function of the brain-specific β4 subunit in CA3 neurons is control of surface trafficking

Fibrodysplasia Ossificans Progressiva: what have we achieved and where are we now? follow-up to the 2015 Lorentz Workshop

Fibrodysplasia ossificans progressiva (FOP) is an ultra-rare progressive genetic disease effecting one in a million individuals. During their life, patients with FOP progressively develop bone in the soft tissues resulting in increasing immobility and early death. A mutation in the ACVR1 gene was identified as the causative mutation of FOP in 2006. After this, the pathophysiology of FOP has been further elucidated through the efforts of research groups worldwide. In 2015, a workshop was held to gather these groups and discuss the new challenges in FOP research. Here we present an overview and update on these topics

Does interhospital transfer improve outcome of acute myocardial infarction? A propensity score analysis from the Cardiovascular Cooperative Project

<p>Abstract</p> <p>Background</p> <p>Many patients suffering acute myocardial infarction (AMI) are transferred from one hospital to another during their hospitalization. There is little information about the outcomes related to interhospital transfer. The purpose of this study was to compare processes and outcomes of AMI care among patients undergoing interhospital transfer with special attention to the impact on mortality in rural hospitals.</p> <p>Methods</p> <p>National sample of Medicare patients in the Cooperative Cardiovascular Study (n = 184,295). Retrospective structured medical record review of AMI hospitalizations. Descriptive study using a retrospective propensity score analysis of clinical and administrative data for 184,295 Medicare patients admitted with clinically confirmed AMI to 4,765 hospitals between February 1994 and July 1995. Main outcome measure included: 30-day mortality, administration of aspirin, beta-blockers, ACE-inhibitors, and thrombolytic therapy.</p> <p>Results</p> <p>Overall, 51,530 (28%) patients underwent interhospital transfer. Transferred patients were significantly younger, less critically ill, and had lower comorbidity than non-transferred patients. After propensity-matching, patients who underwent interhospital transfer had better quality of care anlower mortality than non-transferred patients. Patients cared for in a rural hospital had similar mortality as patients cared for in an urban hospital.</p> <p>Conclusion</p> <p>Transferred patients were vastly different than non-transferred patients. However, even after a rigorous propensity-score analysis, transferred patients had lower mortality than non-transferred patients. Mortality was similar in rural and urban hospitals. Identifying patients who derive the greatest benefit from transfer may help physicians faced with the complex decision of whether to transfer a patient suffering an acute MI.</p

Serum Lipopolysaccharide Binding Protein Levels Predict Severity of Lung Injury and Mortality in Patients with Severe Sepsis

Background: There is a need for biomarkers insuring identification of septic patients at high-risk for death. We performed a prospective, multicenter, observational study to investigate the time-course of lipopolysaccharide binding protein (LBP) serum levels in patients with severe sepsis and examined whether serial serum levels of LBP could be used as a marker of outcome. Methodology/Principal Findings: LBP serum levels at study entry, at 48 hours and at day-7 were measured in 180 patients with severe sepsis. Data regarding the nature of infections, disease severity, development of acute lung injury (ALI) and acute respiratory distress syndrome (ARDS), and intensive care unit (ICU) outcome were recorded. LBP serum levels were similar in survivors and non-survivors at study entry (117.4±75.7 µg/mL vs. 129.8±71.3 µg/mL, P = 0.249) but there were significant differences at 48 hours (77.2±57.0 vs. 121.2±73.4 µg/mL, P<0.0001) and at day-7 (64.7±45.8 vs. 89.7±61.1 µg/ml, p = 0.017). At 48 hours, LBP levels were significantly higher in ARDS patients than in ALI patients (112.5±71.8 µg/ml vs. 76.6±55.9 µg/ml, P = 0.0001). An increase of LBP levels at 48 hours was associated with higher mortality (odds ratio 3.97; 95%CI: 1.84–8.56; P<0.001). Conclusions/Significance: Serial LBP serum measurements may offer a clinically useful biomarker for identification of patients with severe sepsis having the worst outcomes and the highest probability of developing sepsis-induced ARDS